Abstract
BackgroundHere, we genetically and antigenically analyzed influenza B viruses (IBVs) isolated in Japan during the 2017‐2018 and 2018‐2019 influenza seasons.MethodsA total of 68 IBVs (61 B/Yamagata/16/88‐like [B/Yamagata]‐lineage and 7 B/Victoria/2/87‐like [B/Victoria]‐lineage) were antigenically and genetically characterized by using hemagglutination inhibition (HI) assays and phylogenetic analysis, respectively. The susceptibility of IBVs to neuraminidase (NA) inhibitors was assessed by using a fluorescence‐based NA inhibition assay.ResultsAll 61 B/Yamagata‐lineage isolates were genetically closely related to B/Phuket/3073/2013, the vaccine strain for these two seasons. Eleven B/Yamagata‐lineage isolates tested were antigenically similar to B/Phuket/3073/2013 by the HI test. Seven B/Victoria‐lineage isolates were genetically closely related to B/Texas/02/2013, the WHO‐recommended vaccine strain for the 2017‐2018 season; however, they were antigenically distinct from B/Texas/02/2013 with an eightfold or 16‐fold difference in HI titer. Of these 7 isolates, 4 possessed a two‐amino‐acid deletion at positions 162 and 163 in hemagglutinin (HA) and the other 3 had a three‐amino‐acid deletion at positions 162‐164 in HA. Importantly, the variants with the three‐amino‐acid deletion appeared to be antigenically different from the B/Colorado/06/2017 virus with the two‐amino‐acid deletion, the vaccine strain for the 2018‐2019 season with a fourfold or eightfold difference in HI titer. One B/Yamagata‐lineage isolate carrying a G407S mutation in its NA showed a marked reduction in susceptibility to zanamivir, peramivir, and laninamivir.ConclusionsThese results highlight the need for continued monitoring for the prevalence of the antigenic variant with the three‐amino‐acid deletion and the variant with reduced NA inhibitor susceptibility.
Highlights
The accumulation of point mutations in the antigenic sites of HA enables viruses to evade host immune responses induced by prior infections or vaccinations, resulting in the emergence of new antigenic variants with epidemic potential.[3,4]
Anti-influenza drugs that inhibit the enzymatic activity of NA are available for the treatment and prophylaxis of influenza; mutations in the NA active site reduce its susceptibility to NA inhibitor drugs, leading to the emergence of drug-resistant variants.[5,6]
We characterized the influenza B viruses isolated in Japan during the 2018-2019 season, even though influenza B viruses circulated at a lower level in this season compared with the previous season
Summary
Influenza is an acute respiratory infectious disease caused by influenza A and B viruses. The accumulation of point mutations in the antigenic sites of HA enables viruses to evade host immune responses induced by prior infections or vaccinations, resulting in the emergence of new antigenic variants with epidemic potential.[3,4]. During the 2017-2018 influenza season, influenza A/H1N1 2009 pandemic (A/H1N1pdm), A/H3N2, and B viruses co-circulated in Japan.[7]. In Japan, the influenza B epidemic of this season was larger than that of the previous nine seasons. We examined the genetic and antigenic properties of the influenza B viruses isolated in Japan during the winter season. We characterized the influenza B viruses isolated in Japan during the 2018-2019 season, even though influenza B viruses circulated at a lower level in this season compared with the previous season
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